Trends in Neurosciences (TRENDS NEUROSCI)

Publisher: Elsevier

Journal description

The breadth of subject areas that fall into the classification of Neuroscience is possibly the widest in the biomedical sciences. As a results, researchers, students and teachers need access to a source of articles that summarise topics of interest outside their own specialities. Trends in Neurosciences (TINS) fulfils that need.In over twenty years TINS has emerged as the leading current awareness journal in the neurosciences (#1 monthly review journal in the ISI SCI Journals Citation Reports® 1996; Impact Factor, 17.755), publishing succinct and readable articles in a monthly magazine format. Short, focused topical reviews make up the core of each issue. News items, meeting reports, commentaries, letters and the most extensive range of neuroscience book reviews are also published, with occasional centrefolds and special thematic issues adding to the variety.The importance of the interface between basic research and clinical applications is emphasised by a regular column reporting on recent advances in our understanding of the general biology of neurological disorders.

Publications in this journal

[Show abstract][Hide abstract]ABSTRACT:
Tau is a microtubule-associated-protein that is sorted into neuronal axons in physiological conditions. In Alzheimer disease (AD) and other tauopathies, Tau sorting mechanisms fail and Tau becomes missorted into the somatodendritic compartment. In AD, aberrant amyloid-β (Aβ) production might trigger Tau missorting. The physiological axonal sorting of Tau depends on the developmental stage of the neuron, the phosphorylation state of Tau and the microtubule cytoskeleton. Disease-associated missorting of Tau is connected to increased phosphorylation and aggregation of Tau, and impaired microtubule interactions. Disease-causing mechanisms involve impaired transport, aberrant kinase activation, non-physiological interactions of Tau, and prion-like spreading. In this review we focus on the physiological and pathological (mis)sorting of Tau, the underlying mechanisms, and effects in disease.

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Unlike the nonexcitable cell membranes that are ubiquitous in all domains of life, excitable membranes are found almost exclusively in animal organisms (Protozoa and Metazoa). Their transient permeability to ion flow makes possible the rapid detection of, and response to, external stimuli, and results in the phenomena that most clearly distinguish fauna from flora: perception, cognition, and motor activity. Interestingly, all known forms of membrane excitability are a consequence of one unique mechanism: the influx of positively charged ions into the normally alkaline cytoplasm. Here, we suggest that the sudden reversal of the membrane potential during the sensory potential and the action potential is an electrostatic disturbance of homeostasis that is the necessary first step in the processes of ‘sentience’ and ‘irritability’.

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Long-term depression (LTD) of the efficacy of synaptic transmission is now recognized as an important mechanism for the regulation of information storage and the control of actions, as well as for synapse, neuron, and circuit development. Studies of LTD mechanisms have focused mainly on postsynaptic AMPA-type glutamate receptor trafficking. However, the focus has now expanded to include presynaptically expressed plasticity, the predominant form being initiated by presynaptically expressed Gi/o-coupled metabotropic receptor (Gi/o-GPCR) activation. Several forms of LTD involving activation of different presynaptic Gi/o-GPCRs as a ‘common pathway’ are described. We review here the literature on presynaptic Gi/o-GPCR-mediated LTD, discuss known mechanisms, gaps in our knowledge, and evaluate whether all Gi/o-GPCRs are capable of inducing presynaptic LTD.

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Stem cell technologies have created new opportunities to generate unlimited numbers of human neurons in the lab and study neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA). Although some disease hallmarks have been reported in patient-derived stem cell models, it is proving more difficult to recapitulate the full phenotypic extent of these disorders. The problem with these stem cell models lies in the disparity between the advanced age of onset of neurodegenerative disorders and the embryonic nature of the in vitro derived cell types. In this review we discuss experimental methods of in vitro aging of neural cell types as a means to elicit late-onset symptoms in induced pluripotent stem cell (iPSC) models of neurodegenerative disease.

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During development, neural circuits are initially generated by exuberant innervation and are rapidly refined by selective preservation and elimination of axons. The establishment and maintenance of functional circuits therefore requires coordination of axon survival and degeneration pathways. Both developing and mature circuits rely on interdependent mitochondrial and cytoskeletal components to maintain axonal health and homeostasis; injury or diseases that impinge on these components frequently cause pathologic axon loss. Here, we review recent findings that identify mechanisms of axonal preservation in the contexts of development, injury, and disease.

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Autophagy is an important biological process that is essential for the removal of damaged organelles and toxic or aggregated proteins by delivering them to the lysosome for degradation. Consequently, autophagy has become a primary target for the treatment of neurodegenerative diseases that involve aggregating proteins. In Huntington disease (HD), an expansion of the polyglutamine (polyQ) tract in the N-terminus of the huntingtin (HTT) protein leads to protein aggregation. However, HD is unique among the neurodegenerative proteinopathies in that autophagy is not only dysfunctional but wild type (wt) HTT also appears to play several roles in regulating the dynamics of autophagy. Herein, we attempt to integrate the recently described novel roles of wtHTT and altered autophagy in HD.

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Developing neuronal circuits often undergo a period of refinement to eliminate aberrant synaptic connections. Inappropriate connections can also form among surviving neurons during neuronal degeneration. The laminar organization of the vertebrate retina enables synaptic reorganization to be readily identified. Synaptic rearrangements are shown to help sculpt developing retinal circuits, although the mechanisms involved remain debated. Structural changes in retinal diseases can also lead to functional rewiring. This poses a major challenge to retinal repair because it may be necessary to untangle the miswired connections before reconnecting with proper synaptic partners. Here, we review our current understanding of the mechanisms that underlie circuit remodeling during retinal development, and discuss how alterations in connectivity during damage could impede circuit repair.

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The function of neural circuits depends on the precise connectivity between populations of neurons. Increasing evidence indicates that disruptions in excitatory or inhibitory synapse formation or function lead to excitation/inhibition (E/I) imbalances and contribute to neurodevelopmental and psychiatric disorders. Leucine-rich repeat (LRR)-containing surface proteins have emerged as key organizers of excitatory and inhibitory synapses. Distinct LRR proteins are expressed in different cell types and interact with key pre- and postsynaptic proteins. These protein interaction networks allow LRR proteins to coordinate pre- and postsynaptic elements during synapse formation and differentiation, pathway-specific synapse development, and synaptic plasticity. LRR proteins, therefore, play a critical role in organizing synaptic connections into functional neural circuits, and their dysfunction may contribute to neuropsychiatric disorders.

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The birth of new neurons in the walls of the adult brain lateral ventricles has captured the attention of many neuroscientists for over 2 decades, yielding key insights into the identity and regulation of neural stem cells (NSCs). In the adult ventricular–subventricular zone (V–SVZ), NSCs are a specialized form of astrocyte that generates several types of neurons for the olfactory bulb. In this review, we discuss recent findings regarding the unique organization of the V–SVZ NSC niche, the multiple regulatory controls of neuronal production, the distinct regional identities of adult NSCs, and the epigenetic mechanisms that maintain adult neurogenesis. Understanding how V–SVZ NSCs establish and maintain lifelong neurogenesis continues to provide surprising insights into the cellular and molecular regulation of neural development.

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